Abstract
Glutamic acid is the main excitatory neurotransmitter acting both in the brain and in peripheral tissues. Abnormal distribution of glutamic acid receptors occurs in skin hyperproliferative conditions such as psoriasis and skin regeneration; however, the biological function of glutamic acid in the skin remains unclear. Using ex vivo, in vivo and in silico approaches, we showed that exogenous glutamic acid promotes hair growth and keratinocyte proliferation. Topical application of glutamic acid decreased the expression of genes related to apoptosis in the skin, whereas glutamic acid increased cell viability and proliferation in human keratinocyte cultures. In addition, we identified the keratinocyte glutamic acid excitotoxic concentration, providing evidence for the existence of a novel skin signalling pathway mediated by a neurotransmitter that controls keratinocyte and hair follicle proliferation. Thus, glutamic acid emerges as a component of the peripheral nervous system that acts to control cell growth in the skin. These results raise the perspective of the pharmacological and nutritional use of glutamic acid to treat skin diseases.
Highlights
Several studies had shown that the skin performs as neuro-endocrine o rgan[8,9,10] and its activities are mainly regulated by local cutaneous factors[9]
We showed that keratinocytes undergo a Gaussian distribution pattern of viability after Glutamic acid (GA) exposure (Fig. 1b,c)
As the 10 mM and 100 mM GA concentrations showed opposite effects in the viability test, we evaluated whether keratinocyte proliferation could be affected after two days of GA exposure (Fig. 1g)
Summary
Several studies had shown that the skin performs as neuro-endocrine o rgan[8,9,10] and its activities are mainly regulated by local cutaneous factors[9]. This interaction between skin and environment factors can regulate Central Nervous System (CNS) functions[11]. NMDA receptors are highly expressed in type I and type II terminal Schwann cells. These cells are circumferentially localized in the bulge border and cover most outer root sheath keratinocytes in the isthmus[4]. Ex vivo and in silico models, we show that GA promotes keratinocyte proliferation and hair follicle growth by mechanisms that involve the control of vascularization and apoptosis
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